AVP is a hormone primarily involved in water transport. This effect has been shown to be mediated by sitmulation of receptors in the renal collecting tubule, so-called V2 receptors. The proposed study is aimed to determine whether arginine vasopressin (AVP) plays a physiologic role in maintaining potassium and acid-base balance in normal human subjects. Specifically, we wish to test the hypothesis that (a) AVP increases both renal potassium and acid excretion by stimulating V2 receptors in the collecting tubule; (b) dietary potassium loading and ammonium cholrdie loading stimulate AVP secretion while dietary potassium deprivation has the opposite effect; and (c) potassium dperivation impairs the kaliuretic response to AVP, while dietary potassium loading enhances it. Thus, alterations in AVP secretion and amplificaiton/suppression of its renal actions are postulated as previously unrecognized mechanisms whereby potassium and acid-base balance are maintained under conditions where dietary intake of potassium and acid are altered. To test this hypothesis, we shall conduct a three-phase study in healthy subjects with normal kidney function. First, we shall determine if AVP increases potassium excretion and distal urinary acidification and explore the mechanism(s) of these effects. Second, the effect of potassium deprivation, potassium loading, and metabolic acidosis on AVP secretion will be assessed by evaluating AVP secretion in response to an acute osmotic stimulus. Third, the effect of potassium surplus and potassium deprivation on the renal potassium excretory and acidification response to the infusion of physiologic amounts of AVP will be assessed.